Quantitative adjustments in the rate of renal sodium excretion constitute the major defense of man's extracellular fluid volume against the potentially disruptive effects of variations in the intake and extrarenal loss of sodium. Derangements of this renal homeostatic mechanism are a hallmark of diseases characterized by the formation of ascites and/or edema. Although effective therapeutic means are available for manipulating the rate of sodium excretion in the majority of edematous patients, considerable ignorance remains as to the mechanisms responsible for the retention of sodium. The aims of the studies under current investigation are (1) to provide new information concerning the intrarenal regulation of sodium excretion in the rat using conventional clearance and microperfusion-micropuncture techniques and (2) to provide new information concerning the effects of experimentally induced alterations in renal hemodynamics on sodium and water handling by both the intact and isolated kidney of the rat. Such information will prove useful for an understanding of the normal mechanisms of pathological sodium retention frequently encountered in clinical medicine. BIBLIOGRAPHIC REFERENCES: Glomerular Filtration. B.M. Brenner, W.M. Deen and C.R. Robertson. In The Kidney. Co-edited by B.M. Brenner and F.C. Rector, Jr. W.B. Saunders Co., Philadelphia. pp. 251-271, 1976. Effects of Some Vasodilator Drugs on Transcapillary Fluid Exchange in the Renal Cortex. C. Baylis, W.M. Deen, B.D. Myers and B.M. Brenner. Amer. J. Physiol. 230:1148-1158, 1976.